From: "Steve Harris" <SBHarris123@ix.netcom.com>
Newsgroups: rec.scuba,sci.med,sci.med.nursing,misc.legal
Subject: Re: Cervical Cancer Risk When Making Woopy / previously: Cervical 
	Cancer is Contagious
Date: Wed, 6 Jun 2001 03:22:11 -0600

"pirhanna" <pirhanna@bellsouth.net> wrote in message
news:3B1D9C94.66A814A0@bellsouth.net...
> There was a very heated exchange a year or two ago concerning whether or
> not Cervical Cancer can be/is transmitted from person to person to person
> to ...
>
> As I recall, there was a rather stronge challenge to a *headline* which was
> posted - meant to bring attention to the big (now really BIG) problem
> regarding the spread of HPV. The headline was "Cervical Cancer is
> Contagious", or ...found to be contagious" or something like that. As you
> state so elequently (in part):  HPV is transmitted, and therefore so is
> Cervical Cancer (and probably rectal and ...). This does not mean that
> everyone who gets HPV will get Cervical Cancer.
>
> (Couldn't have said it better myself - and didn't)
>
> Concerning: "Cervical Cancer is Contagious"...
> The author was pelted appropriately for his rather audacious,
> headline-style announcement, an announcement that - we can be sure - many
> thousands of women wish they had read.


Yep. It's hard enough to get people to understand the idea of a
multifactorial diseases and risk factors. When the risk factors are
contageous, it really gets hard.

HPV is a really big part of cervical cancer risk, though. It's a bigger
contributor to cervical cancer than smoking is to lung cancer. How about if
we put it that way?

SBH

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med
Subject: Re: A Vaccine for Cervical Cancer...?
Date: Fri, 29 Nov 2002 20:57:17 -0700
Message-ID: <as9cv0$366$1@slb3.atl.mindspring.net>

"Coyotedave" <Coyotedave_member@newsguy.com> wrote in message

>
> Addendum.....
>
> I first heard this story, listening to an P.R.I ( Public
> Radio,International) radio broadcast, on a public broadcast radio
> station.
> That is, I heard that scientist think they were on track to building a
> Vaccine for Cervical Cancer, and that they were assuming that the
> disease was caused by a virus. The information was broadcasted very
> matter of factly, as if Cervical cancer is indeed caused by a virus, and
> that a vaccine they were developing would cure it.

COMMENT:

Cervical cancer is caused by a virus, in the sense that it is never seen in
the absense of HPV viral DNA. Which means that women cannot get cervical
cancer without HPV infection first-- somethat that was borne out long ago
when scientists noticed the virgin nuns never (ever) got cervical cancer.

Having said that, cervical cancer is the only human cancer I know about that
100% requires a virus, unless you count Kaposi's sarcoma as a cancer. Most
other cancers associated with viruses are sometimes also seen in the absense
of the virus, so the virus is risk factor, but not a *necessary* one.
Cervical cancer is different. HVP is a necessary but not sufficient cause of
cervical cancer (not all women infected get cancer).

Now, HPV comes in many strains, some of which cause genital warts, and
others cause cervical infections and cancers (basically strains that do one
thing don't do the other).
The question was whether or not infection by a strain of virus could be
prevented by a vaccine, and that is what was just shown. HPV 16 was
targetted because it causes about half of cervical cancers (just two
strains, 16 and 18, between them cause 70% of cervical cancers). This virus
infects about 20% of women. In a randomized trial of uninfected women,
something like 40 women picked up the virus during the study who'd gotten
the placebo, vs NO women in the vaccine group. Thus, the vaccine was close
to 100% effective at preventing infection.

We can only presume it prevents cervical cancer, but there's no reason to
doubt it. This one vaccine alone should prevent 50% of cases. A nice
bivalent vaccine which prevents HVP-18 also, should prevent 70% of cases.
One day, eventually, pap smears will no longer be necessary, as we will have
wiped out all cancer causing strains of HPV, just as we did smallpox. HVP
isn't something you can get from animals, and neonatal transmission appears
to be rare. So it's a good target to be erradicated by a vaccine.

SBH

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med
Subject: Re: A Vaccine for Cervical Cancer...?
Date: Sat, 30 Nov 2002 13:34:24 -0700
Message-ID: <asb8it$asa$1@slb9.atl.mindspring.net>

"yelxol" <willlocksley@aol.com> wrote in message
news:a71be19b.0211300745.2f08d2cf@posting.google.com...
> > Cervical cancer is caused by a virus, in the sense that it is never seen in
> > the absense of HPV viral DNA. Which means that women cannot get cervical
> > cancer without HPV infection first-- ...
>
> This is a specific area I would like to magnify a bit.
> The most recent studies I have seen use a 99.8% number. I have assumed
> there must be an error rate considered (of poss. +/- at least 1%?),
> which would - statistically - raise the lever to 100%. Obviously, any
> false neg. involving the .2% would fall in favor of the 99.8%, adding
> even more assurance of a 100% reliability. (What do you think here.
> Should/could we simple say that ALL cc has been proven to be
> associated with HPV, or always add the caveat re. the 99.8% / the .2%
> / etc?)

COMMENT:

The study you're thinking about probably, is appended below, and gives the
figure 99.7%, because of a couple of "adequate" speciments in which no HPV
DNA could be found. However, the PCR test for this DNA is not 100%
sensitive, and I think it would take thorough analysis of at least one
large-volume tumor by several methods to insure that somebody has found any
genuine cervical cancer in which there simply cannot reasonably be any HPV
DNA. When you get to numbers like 99.7%, it's rather perverse not to assume
it's probably 100%, and the test occasionally fails. Yes, there's always
room for a very occasional exception. Never say "never" in biology. If you
want to say that HPV is a necessary factor in 99.7% of cervical cancer, I
can't argue. But my guess, at this point, is that it's 100%.


> > ...scientists noticed the virgin nuns never (ever) got cervical cancer.
>
> I have read in several studies that 'confirmed' virgins were found
> with one of the cancer-causing HPV strains. What is your opinion here?
> ( I would like to discuss my thoughts regarding the reasons.)

I'd like to see the studies of virgins with cervical HPV. I'm aware of one
single report in German claiming to have found a 17 yo virgin with cervical
cancer, but since I don't read German I can't evaluate it. I'm skeptical.
There have been a few pregnant virgins, inasmuch as there are ways semen can
get into vaginas even without full intercourse. And presumably HPV also
(even more so the HVP strains that infect the outer genital area, though
these are generally not the ones causing cervical cancer, as noted). What
we'd really like to know is whether the 17 yo German virgin who had cervical
carcinoma, also had no HPV.


> > HVP is a necessary but not sufficient cause of
> > cervical cancer (not all women infected get cancer).
>
> But isn't this the 'pattern' of many other viruses, that one can
> contract a pathogen, but not necessarily progress to present with
> 'full blown' symptoms.

Yes, of course.



> > HPV 16 was
> > targetted because it causes about half of cervical cancers (just two
> > strains, 16 and 18, between them cause 70% of cervical cancers).
>
> I am not so sure this is why 16 was targeted.

Well, why aren't you?  All reports for many years have shown that HPV-16 is
the single strain likely to be responsible for the most cervical cancers.
This was true long before the vaccine companies got involved.


> > This virus infects about 20% of women.
>
> Do you re. to HPV (all 100+ strains) or to GHPV or to HPV-16. (Just
> trying to understand.)

It varies from country to country and socioeconomic group to group and age
to age. But very roughly 20% of adult women eventually become infected with
HPV-16 in the US. For all HPV's the figure is higher-- perhaps 50%.


> > In a randomized trial of uninfected women, something like 40 women
> > picked up the virus during the study who'd gotten the placebo, vs NO
> > women in the vaccine group. Thus, the vaccine was close to 100%
> > effective at preventing infection.
>
> I, of course, understand the term randomized; however, do you recall
> from where this group was selected. IOW, were they from some part.
> group of clinics or a specific city or area of a city, or ????

Not offhand. It's a group of about 2400 young uninfected women, and the
study is from Seattle, WA. I imagine they're all from there, or near there,
but am not sure. Why?

> However, a very real danger as far as misinformation to women. The
> headlines are about as far as some read. And the evening news gave
> their usual bullets, lead with THERE IS NOW A CURE FOR CC. Yes, that
> was the impression left.

Well, that's not my problem, or the medical profession's problem. It's a
problem for journalism and the uneducated public, as explained in another
message.

> I have asked LOTS of women, and that is indeed what they *heard*.
> Not to be TOO cynical, but you can rest assured that the drug
> company's stock did well. Since the 'whispers' of the vaccine started
> in July, Merck's stock has gone up 20 points - or from ~40 to ~60...
> or 50%. (not bad)

And that's the SEC's problem. What, you think all investors are geniuses?

> > HVP
> > isn't something you can get from animals,
>
> Are we sure? What about HPV-77?

What about it? They don't call them "human papilloma viruses" for nothing.


J Pathol  1999 Sep;189(1):12-9

Comment in:
 J Pathol. 1999 Sep;189(1):1-3

Human papillomavirus is a necessary cause of invasive cervical cancer
worldwide.

Walboomers JM, Jacobs MV, Manos MM, Bosch FX, Kummer JA, Shah KV,
Snijders PJ, Peto J, Meijer CJ, Munoz N.

Department of Pathology, University Hospital Vrije Universiteit,
Amsterdam, The Netherlands. JMM.Walboomers@azvu.nl

A recent report that 93 per cent of invasive cervical cancers worldwide
contain human papillomavirus (HPV) may be an underestimate, due to sample
inadequacy or integration events affecting the HPV L1 gene, which is the
target of the polymerase chain reaction (PCR)-based test which was used.
The formerly HPV-negative cases from this study have therefore been
reanalyzed for HPV serum antibodies and HPV DNA. Serology for HPV 16
VLPs, E6, and E7 antibodies was performed on 49 of the 66 cases which
were HPV-negative and a sample of 48 of the 866 cases which were
HPV-positive in the original study. Moreover, 55 of the 66 formerly
HPV-negative biopsies were also reanalyzed by a sandwich procedure in
which the outer sections in a series of sections are used for
histological review, while the inner sections are assayed by three
different HPV PCR assays targeting different open reading frames (ORFs).
No significant difference was found in serology for HPV 16 proteins
between the cases that were originally HPV PCR-negative and -positive.
Type-specific E7 PCR for 14 high-risk HPV types detected HPV DNA in 38
(69 per cent) of the 55 originally HPV-negative and amplifiable
specimens. The HPV types detected were 16, 18, 31, 33, 39, 45, 52, and
58. Two (4 per cent) additional cases were only HPV DNA-positive by E1
and/or L1 consensus PCR. Histological analysis of the 55 specimens
revealed that 21 were qualitatively inadequate. Only two of the 34
adequate samples were HPV-negative on all PCR tests, as against 13 of the
21 that were inadequate ( p< 0.001). Combining the data from this and the
previous study and excluding inadequate specimens, the worldwide HPV
prevalence in cervical carcinomas is 99.7 per cent. The presence of HPV
in virtually all cervical cancers implies the highest worldwide
attributable fraction so far reported for a specific cause of any major
human cancer. The extreme rarity of HPV-negative cancers reinforces the
rationale for HPV testing in addition to, or even instead of, cervical
cytology in routine cervical screening. Copyright 1999 John Wiley & Sons,
Ltd.

Publication Types:
Multicenter Study

PMID: 10451482 [PubMed - indexed for MEDLINE]

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med
Subject: Re: Entire Medical Profession Quietly Ignores Their Own Theory of HPV 
	Dormancy
Date: Mon, 3 Mar 2003 12:05:51 -0800
Message-ID: <b40cmq$oav$1@slb4.atl.mindspring.net>

> Entire Medical Profession Quietly Ignores Their Own Theory of HPV
> Dormancy
> [From &#8220;FATAL PROBE: Are Doctors Cross-Infecting Women With HIV,
> HPV, HSV, HCV, CJD and Other Pathogens?]
> Hopefully, the Merck HPV vaccine will prove to be a successful first
> step in the prevention of infection from all harmful HPV strains. The
> author is not a proponent of the baseless HPV Dormancy claim; therefore,
> dormancy is not expected to become a mitigating factor in the study. The
> hypocrisy of the medical profession &#8211; with regard to this subject
> &#8211; is a separate issue.


Hello?  "Dormancy" is with regard to clinical infection by
genital wart-causing strains of HPV (clinical infection =
warts pop out). These are not, in general, the same strains
that cause cervical cancer. The DNA test finds all HPV
infections, warts or no, which is WHY we can say that 99.3+%
and perhaps 100% of cervical cancers are caused by certain
strains of (non-wart causing) HPV. Most of these women don't
have any infection which is detectable in any other way.
Also, the DNA test allows us to tell the carriage rates for
HPV of the cancer-causing type in the normal population,
even though these are mostly asymptomatic.

The vaccine trials documented infection, or lack of
infection, by DNA testing. I can find no evidence that ANY
of the women in the study got actual genital warts from the
HPV strain in question, and this includes even those who DID
get a new infection with a cancer-causing HPV strain during
the study. The dormancy issue is completely irrelevent, and
you've mistaken the "hypocrisy" of the medical profession
for your own ignorance of the subject here.

SBH


--
Spammers are not welcome. I welcome email
from all non-advertisers who can fix my email
address (it's open book).

From: "Steve Harris" <sbharris@ix.RETICULATEDOBJECTcom.com>
Newsgroups: sci.med
Subject: Re: Entire Medical Profession Quietly Ignores Their Own Theory of HPV 
	Dormancy
Date: Tue, 4 Mar 2003 12:13:25 -0800
Message-ID: <b431h0$sf$1@slb2.atl.mindspring.net>

"yelxol" <willlocksley@aol.com> wrote in message
news:a71be19b.0303041109.741e5438@posting.google.com...

> Are you implying that the HPV strains that cause cc are not included
> in the Dormancy Theory that is claimed so widely?



More or less correct. If they don't cause visible infection,
how can one tell if they are dormant or not? I think most
specialists assume that the cancer-causing strains have
active and dormant periods just as the wart-causing strains
do, but it hasn't been proven. In any case, DNA testing
finds the HPV virus whether it is dormant or not, no matter
what strain it is. Dormant virus still sits in the cell as
DNA, and so is detectable. So the issue is irrelevent to
whether or not the vaccine works to prevent infections. It
works.


> And are you suggesting this because &#8211; as you say &#8211; the HPV
> strains that cause cc are not associated with warts?
>
> Best regards.

I'm saying it because the method of detection used in the
vaccine trials makes dormancy an irrelevant issue.

SBH



--
Spammers are not welcome. I welcome email
from all non-advertisers who can fix my email
address (it's open book).

From: sbharris@ix.netcom.com (Steve Harris  sbharris@ROMAN9.netcom.com)
Newsgroups: sci.med
Subject: Re: CERVICAL CANCER IS AN INFECTIOUS DISEASE. Ch V. FATAL PROBE
Date: 7 Feb 2004 14:08:49 -0800
Message-ID: <79cf0a8.0402071408.2d902052@posting.google.com>

willlocksley@aol.com (yelxol) wrote in message
news:<a71be19b.0402060617.664361d8@posting.google.com>...

> Beginning with medical school, physicians are taught to never tell a
> patient they do not know the answer to a patient's question,


Comment:

Bullshit. Burdon of proof for this outrageous statement rests on you.
Why do you you think it's true? Can you find it in any published
material for any medical school curricula? Have you heard it while
attending medical school (I haven't, and what's more I've been there
to hear it, and you haven't). You have a tape recording of medical
students being told this in medical school? No? So what's your
evidence?



> However, let us be perfectly clear on this?
> There is credible evidence that shows the medical profession
> manufactured this myth and set in place a methodical plan of action as
> a scheme to cover up the very real probability that large numbers of
> women have become, and continue to become, infected with
> cancer-causing HPV in their medical providers' office environments.


COMMENT:

There is no such credible evidence. In fact, it sounds like paranoid
ravings. As does any theory which requires that millions of physicians
and nonphysician virologists alike are "in on" some vast conspiracy.
Which only you seem to know about, at this point.


> In
> fact:
>
> No study exists that demonstrates HPV remains dormant in the human
> body for decades!

COMMENT:

Define your terms. "Dormant" is not a medical word, and is only used
by doctors in trying to explain medical terms like subclinical or
latent. Probably "dormant" is a bad synonym because no viral
infection, even one which shows no outward signs, is ever truely
dormant. Even herpes zoster, waiting decades between chickenpox and
shingles, is ticking over and making at least one protein. Think of it
rather like that fog that the eggs make in the movie Alien.

The idea of latency of infections for "decades" is an extrapolation of
studies which have found evidence of latency of HPV infections for
longer than 5 years in serial followup studies. Longer periods are
extrapolated from that, since it seems reasonable to imagine that
women who've been infected for more than years (and as long as the
study has run) with the same strains of HPV, will remain infected for
longer than that, as well. Here is a study which was running for 8
years at the time it was reported, and long latency is what it
concluded:


APMIS. 1989 Nov;97(11):957-70.

Epidemiology of human papillomavirus (HPV) infections and their
associations with genital squamous cell cancer. Review article.

Syrjanen KJ.

Department of Pathology, University of Kuopio, Finland.

Reliable assessment of the epidemiology of genital HPV infections is
hamphered by a number of technical problems. Because of the lack of
tissue-culture systems, methods based on morphological approaches
(colposcopy, cytology and histopathology) play a central role in HPV
diagnosis. Even DNA-hybridization techniques and the recently
introduced DNA amplification with PCR are extremely difficult to
standardize, and are thus subject to major interlaboratory variation.
Further confusion in the field is created by the complex biological
behaviour of HPV infections. As established by the long-term
prospective follow-up study of over 500 women which has been running
in Kuopio since 1981, clinical progression and regression are
significantly related to the grade of the lesion at the time of
diagnosis (p less than 0.00001, and p = 0.0005, respectively), as well
as to the type of HPV (p = 0.0012). Most importantly, however, genital
HPV infections seem to run an extremely fluctuating course, passage
from manifest to subclinical or latent infection being frequently
encountered in individual patients when examined at 6-month intervals
over prolonged periods. This explains the significantly divergent
prevalence figures reported in different series (ranging from 2% to
80%), which are completely dependent on the technique used to analyse
the presence of HPV, i.e. whether a) PAP smear, b) biopsy, c) DNA
hybridization, or d) PCR amplification. The first two are capable of
disclosing only manifest (clinical) infections, the latter two also
the latent ones. In an unselected population of 22-year-old Finnish
females, the prevalence of clinical HPV infections was about 3 per
cent, and the adjusted annual incidence was 8.0 per cent. According to
estimates of the life-time risk, up to 79% of Finnish females will
contract at least one HPV infection between the ages 20 to 79 years.
When related to the long-term trends in invasive cervical cancer in
Finland, it is evident that this 79% life-time risk of becoming
HPV-infected or even the observed 15% clinical progression rate for
HPV infections in the prospective follow-up study by no means
signifies an identical risk of developing cervical cancer (i.e. 0.79 x
0.15 = 11%). It seems likely that in countries where mass-screening
programmes exist (and precancer lesions are traced), the high
prevalence of HPV infections is not necessarily reflected as an
increased prevalence of invasive cervical carcinomas. The distinction
of lesions at risk for malignant transformation from those regressing
spontaneously will have major implications in therapeutic
considerations of genital HPV infections.

Publication Types:
Review
Review Literature

PMID: 2556164 [PubMed - indexed for MEDLINE]



> The fundamental mechanics necessary for such a study extend the
> imagination beyond the limits of credulity, with the major dilemma in
> managing such a project being the re-infection component, a completely
> unmanageable control factor for human subjects.


COMMENT:
Quite so, but one presumes that when there are close correlations
between strains of latent virus detected, and previous non-latent
infections years before, that this is not a coincidence. Yes, perhaps
it's reinfection by the same partner. However, HPV is a long latency
virus in animal models as well, where one can control for these
factors. YOUR hypothesis is that it behaves completely differently in
humans. I think the more likely hypothesis is that it does in people
what it does in other primates.

It is also possible that HPV is spread by routes other than sexual. If
it's non-sexual, that doesn't mean foreign objects are all that are
left. The virus may well be transmitted vertically, from mother to
daughter, at birth.

Consider the following:

Dev Biol (Basel). 2001;106:443-51; discussion 452-3, 465-75.

Viral latency--the papillomavirus model.

Broker TR, Jin G, Croom-Rivers A, Bragg SM, Richardson M, Chow LT,
Vermund SH, Alvarez RD, Pappas PG, Squires KE, Hoesley CJ.

Department of Biochemistry and Molecular Genetics, University of
Alabama at Birmingham, 35294-0005, USA.

To investigate the prevalence and the natural history of human
papillomavirus infections, we monitored HPV DNA shedding as a
consequence of immunosuppression, with the expectation that latent
viral infections would reactivate and become detectable. The study
populations consisted of women who were in end-stage renal failure,
those who ultimately received kidney transplantations, and those who
had HIV/AIDS with various degrees of immune depression at entry. For
each woman, cervico-vaginal lavage to sample viral shedding from the
lower genital tract was performed at approximately six month
intervals, and the cohorts have been followed since 1996. Nested
polymerase chain reaction amplification of papillomavirus DNA using
novel pairs of primers was followed by diagnostic restriction
endonuclease cleavage or by DNA sequencing. This strategy is
particularly capable of identifying single and multiple infections and
determining the genotypes of any viruses present. Of the 225 women in
the HIV cohort, 177 (79%) were HPV-positive and 111 (49%) shed from
two up to eight different HPV types over the course of the survey.
Thirty-five different mucosotropic HPV types, virtually all that have
ever been described worldwide, were isolated from these 225 women, and
nine additional new (provisional) types were discovered. As is always
the case, HPV-6 was very common. However, all the other frequently
detected HPV types (45, 52, 53, 54, 58, 74) were more prevalent than
the types typically reported forthe general population (HPV-11, 16,
18, 31, 33, 35). Notably, the 14 members of the A3 phylogenetic
subgroup (HPV-61, 62, 72, 81, 83, 84, and all the new types) were by
far the most frequently observed viral types in the AIDS cohort. The
HPV prevalence in the cohorts of kidney transplantation candidates and
recipients was only slightly lower than that in the AIDS cohort. We
conclude that HPV infections are extraordinarily common and are
normally held in a sub-clinical state by functional immune systems,
but can be reactivated by immunosuppressive conditions. The question
of how so many distinct types persist in the human population and can
be repeatedly isolated from specimens collected around the world
raises complex issues concerning the nature of viral transmission,
reproduction, shedding, and mutational drift. These molecular
epidemiological observations signal the likelihood that HPV is part of
the commensal microflora of human epithelia. Their prevalence elicits
a caution that latent HPV DNA may be present in primary human
epithelial tissues.


> Nevertheless, regardless of the fact that there is no basis for the
> dormancy theory, the surge of "medical hearsay" that parrots this
> beguiling Medspeak dominates the Internet landscape. Approximately
> 1,500 web sites ? most associated with the medical community ? claim,
> affirm and reaffirm this misconception, which is now spewed from the
> mouths of ignorant physicians and nurses.

COMMENT:
And also "spewed" the mouths of people who've spent their professional
careers working with this virus, and who've forgotten more about it
than YOU will ever know. But you are here saying you know better. On
what grounds? Where are your studies? The ones you quote do not
support your position. What are your credentials? Hell, what is your
name? If you want to talk "hearsay," your essays serve as wonderful
examples.



> In the most favorable light, this scheme underlines the fact that the
> practice of medicine is not a science.

COMMENT
It is an applied science, like engineering. Like engineering, there is
some art to it.

> Although physicians and other medical providers assert long-term HPV
> dormancy as though it is a proven fact, it is important that the
> public knows the truth:
>
> There is much credible evidence to support the converse, that:
> HPV does not remain dormant in the human body for several years, and
> certainly not for decades or for a person's lifetime.

COMMENT:
No, there isn't. There is evidence that it may not remain in the
bodies of SOME people. That doesen't mean it doesn't in "many" or even
"most." Finding that some women clear the virus does not mean that all
do, or even that most do.

> Several studies have been conducted for the purpose of determining
> whether HPV remains dormant. Although they are doomed from the outset
> ? based on the above reasoning ? all of them concluded on the side of
> the fact that HPV does not remain dormant.

COMMENT:
No, that is incorrect. I have posted two to the contrary in this
message alone (see above). So much for your use of the word "all."


> Here is a summary of a report by "Infectious Disease News" concerning
> the latest study:
> ..."It has long been suggested that all HPV infections result in
> lifelong carriage of the organism and that the virus may remain
> "clinically silent," but a 1993 study, and the recently completed
> follow-up study, produced contrasting results, according to lead
> author Anna-Barbara Moscicki, MD, Univ of California at San Francisco.
> ...The first study suggested that ***some*** [italics added by SBH,
> since somebody else seeems to have missed this word] women infected with
> HPV appear to eliminate the infection over a short time and are at low
> risk ? or no risk ? of developing disease. The newest study yielded even
> more promising results.
> ...Approximately 300 age-eligible women were screened?
> ...Based on the original 1993 study, the women were followed for a
> mean of 27.6 months with an average of six visits?
> ...Moscicki said (the study) suggests that the cervices of patients
> with repeatedly negative PCR results are free of the HPV types tested
> and that the women had neither latent nor active HPV cervical
> infection."
> ...Variability of (HPV) DNA testing in a longitudinal cohort of young
> women; Moscicki AB, et.al.; Obstet Gynecol 1993 Oct;82(4 Pt 1):578-85


COMMENT:

And what fraction of women in the study was this?  Let's see if you
can read.


SBH

From: sbharris@ix.netcom.com (Steve Harris  sbharris@ROMAN9.netcom.com)
Newsgroups: sci.med
Subject: Re: CERVICAL CANCER IS AN INFECTIOUS DISEASE. Ch V. FATAL PROBE
Date: 8 Feb 2004 15:47:55 -0800
Message-ID: <79cf0a8.0402081547.37539918@posting.google.com>

willlocksley@aol.com (yelxol) wrote in message
news:<a71be19b.0402081009.5099478@posting.google.com>...
> Steve / Dr. Harris:
>
> Thanks for your review of this post.
>
> First. I think it was a bit 'out of bounds' to insert question marks
> within my posts. But... the foul didn't 'determine the outcome of
> the...'; therefore, I overlook it... sort of.
>
> ex.:
> > ...Based on the original 1993 study, the women were followed for a
> > mean of 27.6 months with an average of six visits?  (your inserted "?")
>
> Definite foul here and in several other spots.



COMMENT:

All of which you'll see happened when the google newsreader ran across
the odd dash symbols in your text which you apparently intend to be
hyphens, and read each as a "?". I didn't figure out at first this was
happening. Which is fine, because neither did you. However, this is a
microcosm for your attitude, because instead of realizing finally that
this was a simple machine error in coding, *you* decided instead that
some doctor, namely myself, was responsible for it, with evil intent.
Which attitude is pretty much is my problem with your whole style of
looking at life. Capiche?

SBH